Ginger Could Improve Gestational Diabetes by Targeting Genes Involved in Nutrient Metabolism, Oxidative Stress, Inflammation, and the WNT/β-Catenin/GSK3β Signaling Pathway

Abstract

This study aimed to evaluate the effect in female rats of 6 weeks of ginger consumption on gestational diabetes by assessing glucose and lipid metabolism, oxidative damage, inflammation, and the WNT/β-catenin/glycogen synthase kinase-3 beta (GSK3β) signaling pathway. In this study, 40 adult female rats were divided into 4 equal groups as follows: pregnant rats, pregnant rats with diabetes, pregnant rats consuming ginger, and pregnant rats with diabetes consuming ginger. Induction of diabetes on day 0 of pregnancy was induced by streptozotocin (STZ) injection. Insulin, glucose, and lipid profiles as metabolic factors were measured along with the hepatic expression of glucose transporter type 4 (GLUT4), mechanistic target of rapamycin complex 1 (mTORc1), sterol regulatory element-binding protein-1c (SREBP-1c), peroxisome proliferator-activated receptor α (PPAR-α), β-catenin, GSK3β, PPAR-g, nuclear factor-κB (NF-kB), and nuclear factor erythroid 2-related factor 2 (Nrf2). The levels of tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β), and oxidative parameters were measured in the liver. The level of metabolic factors was significantly impaired in diabetic pregnant rats compared to the control group. However, ginger improved these parameters in the diabetic pregnant—ginger group compared to the diabetic pregnant group. The hepatic expression of genes involved in metabolism, oxidative stress, inflammation, and the wingless and int-1 (WNT) signaling pathway was significantly impaired in diabetic pregnant rats, while ginger improved them in the hepatic tissue of diabetic pregnant rats. It can be concluded that ginger could improve gestational diabetes by genes involved in metabolism, the WNT signaling pathway, oxidative stress, and inflammation. These results suggest that ginger can be an adjunct drug during pregnancy as a metabolic modulator.